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NFKB1 — TLR3
Text-mined interactions from Literome
Horng et al., Nat Immunol 2001
:
Although some cellular responses are completely abolished in MyD88-deficient mice,
TLR4 , but not TLR9, can
activate NF-kappa B and mitogen activated protein kinases and induce dendritic cell maturation in the absence of MyD88
Alexopoulou et al., Nature 2001
(Virus Diseases) :
Recognition of double stranded RNA and
activation of
NF-kappaB by
Toll-like receptor 3 ... Here we show that mammalian
TLR3 recognizes dsRNA, and that activation of the receptor
induces the activation of
NF-kappaB and the production of type I interferons ( IFNs )
An et al., Immunology 2002
:
While inhibition of extracellular signal related kinase and
NF-kappaB activation
suppressed the up-regulation of the expression of TLR2,
TLR4 and TLR9 mRNA, inhibition of p38 kinase prevented the up-regulation of TLR2 and TLR4 mRNA expression but enhanced the up-regulation of TLR9 expression
Takami et al., J Immunol 2002
:
Moreover, various
TLR ligands ( e.g., peptidoglycan, poly ( I:C ) dsRNA, LPS, and CpG motif of unmethylated DNA, which act as ligands for TLR2, 3, 4, and 9, respectively )
induced NF-kappa B activation and up-regulated TNF-alpha production in osteoclast precursor cells
Zhang et al., FEBS Lett 2002
:
NF-kappaB activation by TLR2/1,
TLR2/6 and the TLR4 monomer, but not TLR4/4, was completely inhibited by dominant negative MyD88, suggesting that TLR4 homodimers and monomers could activate NF-kappaB through different mechanisms
Jiang et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
However, we find that, in response to dsRNA,
TLR3 can
mediate the activation of both
NFkappaB and mitogen activated protein ( MAP ) kinases in IL-1-unresponsive mutant cell lines, including IRAK-deficient I1A and I3A cells, which are defective in a component that is downstream of IL-1R but upstream of IRAK
Fitzgerald et al., Nat Immunol 2003
(Virus Diseases) :
Viral infection, or the binding of double stranded RNA to
Toll-like receptor 3 ,
results in the coordinate activation of IRF3 and
NF-kappaB
Akira et al., J Infect Dis 2003
:
After stimulation,
TLR recruits IL-1R associated kinase via adaptor myeloid differentiation factor 88 ( MyD88 ) and
induces activation of
NF-kappaB and mitogen activated protein kinases
Janssens et al., FEBS Lett 2003
:
MyD88 is an adapter protein that is involved in
Toll-like receptor ( TLR ) - and interleukin-1 receptor (IL-1R) induced
activation of
nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) ... MyD88 ( S ) is not able to activate NF-kappaB, and in contrast functions as a dominant negative inhibitor of
TLR/IL-1R induced
NF-kappaB activation
Jiang et al., Proc Natl Acad Sci U S A 2004
:
Toll-like receptor 3-mediated activation of
NF-kappaB and IRF3 diverges at Toll-IL-1 receptor domain containing adapter inducing IFN-beta ... Recently, a novel Toll-IL-1 receptor ( TIR ) -containing adapter, TIR domain containing adapter inducing IFN-beta ( TRIF ), was shown to play a critical role in
TLR3 mediated
activation of
NF-kappaB and IRF3 ... Interestingly, mutation of the TRAF6 binding site of TRIF only abolished its ability to activate NF-kappaB but not IRF3, suggesting that
TLR3 mediated
activation of
NF-kappaB and IRF3 might bifurcate at TRIF
Meylan et al., Nat Immunol 2004
:
Analysis of Trif-deficient mice has shown that
TLR3 dependent activation of the transcription factor
NF-kappa B by the TLR3 ligand double stranded RNA is Trif dependent
Akira et al., C R Biol 2004
:
Upon stimulation,
TLR recruits a cytoplasmic adaptor molecule MyD88, then IL-IR associated kinase ( IRAK ), and finally
induces activation of
NF-kappaB and MAP kinases
Pivarcsi et al., Acta Microbiol Immunol Hung 2004
:
In response to challenge with microbes or microbial derived substances the activation and nuclear translocation of
NF-kappaB , the production of nitric oxide ( NO ) and inflammatory cytokines occur in keratinocytes, in a
TLR dependent manner
Seki et al., Hepatology 2005
:
However,
TLR2 , 4 and 9, which recognize gram negative and -positive bacterial products, are not
essential for
NF-kappaB activation and IL-6 production after PH, which excludes a possible contribution of TLR2/TLR4 or TLR9 to MyD88 mediated pathways
Bucki et al., Biochemistry 2005
:
Additionally,
TLR dependent
NF-kappaB translocation in astrocytes appears to be blocked by gelsolin
Okahira et al., DNA Cell Biol 2005
:
Toll-like receptor (TLR) 3 , a member of TLR family proteins, recognizes extracellular dsRNA and
activates NF- kappaB and the IFN-beta promoter leading to the induction of IFN-beta production
Abujamra et al., Virology 2006
:
Using Toll-like receptor ( TLR ) deficient HEK293 cells and PKR ( -/- ) mouse embryo fibroblasts, we further demonstrate that although dsRNA activated protein kinase R (PKR) is not necessary,
TLR3 is
required for the activation of
NFkappaB by the LTR
Su et al., Eur J Immunol 2006
:
Overexpression of TRAF1 inhibited TRIF- and
TLR3 mediated
activation of
NF-kappaB , IFN stimulated response element and the IFN-beta promoter
Yamaguchi et al., FEBS Lett 2005
:
Therefore, in the present study, we investigated whether globular adiponectin ( gAd ) would be able to inhibit
TLR mediated
nuclear factor-kappaB (NF-kappaB) signaling in mouse macrophages ( RAW264 ) ... gAd predominantly bound to the AdipoR1 receptor and suppressed
TLR mediated
NF-kappaB signaling ... gAd mediated inhibition of
TLR mediated IkappaB phosphorylation and
NF-kappaB activation was eliminated by the pretreatment of cycloheximide
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating
Toll-like receptor ( TLR ) -interleukin 1 receptor (IL-1R) signaling and subsequent
activation of
NF-kappaB and AP-1, transcriptional activators of innate immunity
Musette et al., Med Sci (Paris) 2006
(Infection...) :
The
TLR activation
induce the
NF-kappaB translocation to the nucleus and cytokine secretion
Sun et al., J Biol Chem 2006
:
Cells treated with tunicamycin, an inhibitor of glycosylation, prevented
TLR3 induced
NF-kappaB activation, confirming that N-linked glycosylation is required for bioactivity of this receptor
Minoda et al., Biochem Biophys Res Commun 2006
:
Overexpression and knockdown by siRNA indicated that ZCCHC11 functions as a negative regulator of
TLR mediated
NF-kappaB activation
Qin et al., J Biol Chem 2006
:
On the other hand,
TLR8 mediated IkappaBalpha phosphorylation,
NF-kappaB , and JNK activation are completely abolished in MEKK3 ( -/- ) MEFs, whereas IL-1 mediated signaling was only moderately reduced in these deficient MEFs as compared with wild-type cells
Takahashi et al., J Vet Med Sci 2006
:
These observations suggest that immediate response of NODs to endotoxins could result from
NF-kappaB activation via
TLR signaling, whereas the second rise in NOD mRNAs might have resulted from TNF-alpha production possibly through NF-kappaB, TLR, and/or NOD signalings
Kataoka et al., Cell Microbiol 2006
:
TLR2 ( N114A, N199A ), TLR2 ( N114A, N414A ) and, to a lesser extent,
TLR2 ( N114A, N442A ), in which two N-linked glycans are speculated to be exposed to the concave surface of TLR2 solenoid, not only
induce NF-kappaB activation but also are associated with wild-type TLR2 and TLR6
Jiang et al., Cell Res 2006
(Respiratory Distress Syndrome, Adult) :
Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through
TLR dependent basal activation of
NF-kappaB
Broad et al., Immunology 2007
:
In this study we have shown that, whilst
NF-kappaB activation and production of TNF-alpha and interleukin-12 by murine RAW264.7 and J774.2 cells in response to stimulation by TLR4, -5, -7 or -9, was reduced by prior stimulation with TLR4, -5, -7 or -9 ligands, the primary stimulation of
TLR3 , which does not use the MyD88 pathway, did not
reduce the TNF-alpha or interleukin-12 responses to subsequent TLR stimulation
Boyd et al., Cardiovasc Res 2006
(Myocarditis) :
Using transfection of a nuclear factor kappa B (NF-kappaB)-Luciferase reporter plasmid, we found significantly increased
NF-kappaB transcriptional activity in
response to TLR2,
TLR4 and TLR5 activation in cardiomyocytes
Ishihara et al., Curr Pharm Des 2006
(Gastrointestinal Diseases...) :
In the intestine,
TLR dependent activation of
NF-kappaB plays a vital role in maintaining epithelial homeostasis as well as regulating infections and inflammation, while dysregulation of TLR signaling is associated with the pathogenesis of inflammatory bowel diseases ( IBD )
Fukuda et al., Nucleic Acids Symp Ser 2006
:
TLR3 mediates the activation of IRF-3 and
NF-kappaB and thereby the secretion of type I interferons and inflammatory cytokines
Asakura et al., Am J Hematol 2007
:
Here we show that ectopic overexpression of catalytically inactive dominant negative PKR expression system suppressed
NF- kappa B activation
mediated by TLR3,
TLR9 , TNF receptor 1 and 2 (TNF-R 1/2), but not by TLR4
Ranjith-Kumar et al., J Biol Chem 2007
:
We also made over 80 mutations in the residues that could affect these features in the full-length TLR3 and examined their effects in
TLR3 mediated
NF-kappaB activation
Shamshiev et al., J Exp Med 2007
(Dyslipidemias...) :
We found that oxidized low-density lipoprotein ( oxLDL ) was the key active component responsible for this effect, as it could directly uncouple
TLR mediated signaling on CD8alpha ( - ) myeloid DCs and
inhibit NF-kappaB nuclear translocation
Carmody et al., Cell Mol Immunol 2007
(Infection) :
Many of the key molecular events required for
TLR induced
NF-kappaB activation have been elucidated
Gringhuis et al., Immunity 2007
:
We demonstrated that pathogens trigger DC-SIGN on human DCs to activate the serine and threonine kinase Raf-1, which subsequently leads to acetylation of the NF-kappaB subunit p65, but only after
TLR induced activation of
NF-kappaB
Karrasch et al., J Immunol 2007
(Colitis...) :
We conclude that bacteria induced experimental colitis involves the activation of
TLR induced
NF-kappaB signaling derived mostly from mucosal immune cells ... Blocking
TLR induced
NF-kappaB activity may represent an attractive strategy to treat immune mediated intestinal inflammation
Weersma et al., Scand J Gastroenterol 2007
(Colitis, Ulcerative...) :
The interleukin receptor associated kinase-M ( IRAK-M ) is a
NF-kappaB mediated , negative regulator of
Toll-like receptor ( TLR ) signaling
Lundberg et al., Blood 2007
(Inflammation) :
Furthermore,
TLR3 stimulation did not
activate NFkappaB , MAPKs, or IRF-3 in DCs and MOs, but was able to do so in ECs and RA-SF
Yamamoto et al., J Exp Med 2007
:
Microarray analysis showed that Trib1-deficient macrophages exhibited a dysregulated expression pattern of lipopolysaccharide-inducible genes, whereas
TLR mediated activation of MAP kinases and
NF-kappaB was normal
Kubo-Murai et al., J Biochem 2008
:
IRAK-4 dependent degradation of IRAK-1 is a negative feedback signal for
TLR mediated
NF-kappaB activation ... These results suggested that the expression of IRAK-4 alone is sufficient to cause the degradation of IRAK-1 ; the autophosphorylation of IRAK-1 is not necessary to terminate the
TLR induced activation of
NF-kappaB
Dogusan et al., Diabetes 2008
:
TLR3 signaling
mediated PICex induced
nuclear factor-kappaB (NF-kappaB) and IRF-3 activation and beta-cell apoptosis
Shi et al., Nat Immunol 2008
:
Our results collectively indicate that TRIM30alpha negatively regulates
TLR mediated
NF-kappaB activation by targeting degradation of TAB2 and TAB3 by a ` feedback ' mechanism
Wilson et al., J Virol 2008
:
We report that expression of WNV NS1 inhibits
TLR3 induced transcriptional activation of the IFN-beta promoter and of an
NF-kappaB-responsive promoter
Xu et al., Mol Immunol 2008
:
PTP1B inhibits
TLR ligands induced
activation of MAPKs,
NF-kappaB , and IRF3, furthermore, co-transfection of PTP1B inhibits both MyD88- and TRIF induced transcription of TNF-alpha and IFN-beta reporter genes in a dose dependent manner
van Keulen et al., Atherosclerosis 2009
(Carotid Artery Diseases...) :
Tlr activation
results in nuclear translocation of the transcription factor
Nuclear Factor-kappa B (NF-kappaB) that controls the transcription of many inflammatory genes
Zheng et al., Infect Immun 2008
:
Taken together, our results demonstrate that Campylobacter induced IL-8 secretion requires functional flagella and CDT and depends on the
activation of
NF-kappaB through
TLR signaling and CDT in human intestinal epithelial cells
Sugiyama et al., Eur J Pharmacol 2008
(Shock, Septic) :
STM28 showed no inhibitory effects against
NF-kappaB activation
induced by TLR1/2,
TLR3 and TLR9 ligands in a mouse macrophage cell line, RAW 264
Fraczek et al., J Biol Chem 2008
:
Two parallel interleukin-1 (IL-1) mediated signaling pathways have been uncovered for
IL-1R-TLR mediated
NFkappaB activation : TAK1 dependent and MEKK3 dependent pathways, respectively ... Deletion analysis of IRAK4 indicates the essential structural role of the IRAK4 death domain in receptor proximal signaling for mediating
IL-1R-TLR induced
NFkappaB activation
Yoneda et al., Int J Oncol 2008
(Carcinoma, Hepatocellular...) :
Dual topology of functional Toll-like receptor 3 expression in human hepatocellular carcinoma : differential signaling mechanisms of
TLR3 induced
NF-kappaB activation and apoptosis
Shin et al., PLoS Pathog 2008
:
This enhanced response involved
NF-kappaB activation by
TLR signaling as well as Nod1 and Nod2 detection of type IV secretion
Shah et al., Neurosci Lett 2009
:
At the molecular level, beta-glucan suppressed
TLR mediated
NF-kappaB activation, which may be responsible for the diminished capacity of microglia to produce cytokines in response to TLR stimulation
Maitra et al., Journal of inflammation (London, England) 2009
:
Activation of the transcription factor
NFkappaB through
Toll-like receptors ( TLR ) following bacterial infection is principally involved in regulating lung inflammation in CF. NFkappaB regulates the transcription of several genes that are involved in inflammation, anti-apoptosis and anti-microbial activity, and hyper-activation of this transcription factor leads to a potent inflammatory response
Zorde-Khvalevsky et al., Hepatology 2009
:
Furthermore, within the first hours, we observed a dramatic
TLR3 dependent
NF-kappaB activation and an increase in Rip3 levels in hepatocytes, accompanied by caspase-8 activation but without an apoptotic outcome
Yoshimi et al., J Immunol 2009
:
Reporter analyses demonstrated that
TLR mediated
NF-kappaB activation was higher in Trim21 ( -/- ) cells than in wild-type cells, most likely accounting for their enhanced cytokine expression
Logunov et al., Mol Gen Mikrobiol Virusol 2009
:
Various strains of mycoplasmas cause activation of transcriptional factor
NF-kB as a
result of interaction with different combinations of
Toll-like receptors ( TLR )
Gao et al., Cell Mol Life Sci 2009
:
Transforming growth factor-beta activated kinase 1 ( TAK1 ) is a serine/threonine protein kinase that is critically involved in the
activation of
NF-kappaB by tumor necrosis factor ( TNFalpha ), interleukin-1beta (IL-1beta) and
TLR ligands
Brownlie et al., Mol Immunol 2009
:
In this study, chicken TLRs 7, 15 and 21 were expressed in mammalian HEK-293T cells ; expression of
TLR21 but not TLR7 or 15
resulted in marked
NF-kappaB activation upon stimulation with exogenous ODN ...
TLR21 mediated
NF-kappaB activation in HEK-293T cells was inhibited by bafilomycin A suggesting that endosomal maturation is required for TLR21 activation and observations by confocal microscopy and digestion with endoglycosidase H suggest TLR21 localizes to the endoplasmic reticulum ( ER ) of resting cells
Verstak et al., J Biol Chem 2009
(Bacterial Infections...) :
We have previously reported an interaction between Mal and tumor necrosis factor receptor associated factor 6 ( TRAF6 ) via a TRAF6 binding motif, the disruption of which inhibited
TLR mediated
NF-kappaB-luciferase reporter activity
Loiarro et al., J Biol Chem 2009
:
Moreover, overexpression of a green fluorescent protein ( GFP ) -tagged mini-MyD88 protein ( GFP-MyD88- ( 27-72 ) ), comprising the Glu ( 52 ) and Tyr ( 58 ) residues, interfered with recruitment of both IRAK1 and IRAK4 by MyD88 and suppressed
NF-kappaB activation by the interleukin-1 receptor but not by the MyD88 independent
TLR3
Huang et al., J Clin Microbiol 2009
:
The assay readout is the induction of
NF-kappaB and/or cytokines in
response to
TLR activation
Chang et al., Nat Immunol 2009
(Inflammation) :
Peli1 was required for
TLR3 induced activation of IkappaB kinase (IKK) and its ` downstream ' target, transcription factor
NF-kappaB , but was dispensable for IKK-NF-kappaB activation induced by several other TLRs and the interleukin 1 (IL-1) receptor
Rydberg et al., Immunology 2009
(Carcinoma, Squamous Cell...) :
In Detroit-562, TLR2 and TLR5 activation was mediated via c-jun N-terminal kinase ( JNK ) -, p38-, phosphatidylinositol 3-kinase (PI3K)- and nuclear factor (NF)-kappaB related pathways, while
TLR3 was
dependent on
NF-kappaB
Lim et al., Am J Physiol Gastrointest Liver Physiol 2009
:
TLR3 mediated
NF-{kappa}B signaling in human esophageal epithelial cells ... Importantly, we also show that poly ( I:C ) stimulation induces the NF-kappaB dependent esophageal epithelial expression of TLR2, leading to enhanced epithelial responsiveness of EPC2-hTERT cells to TLR2 ligand stimulation, suggesting an important regulatory role for
TLR3 mediated
NF-kappaB signaling in the innate immune response of esophageal epithelial cells ... Our findings demonstrate for the first time that TLR3 is highly functional in the human esophageal epithelium and that
TLR3 mediated
NF-kappaB signaling may play an important regulatory role in esophageal epithelial homeostasis
He et al., Clinical and vaccine immunology : CVI 2009
(Mycoplasma Infections) :
The activity of
NF-kappaB was synergically
augmented by cotransfected TLR1,
TLR6 , and CD14
Boyd et al., J Immunol 2009
:
Specifically, we demonstrate the Siglec-E expression inhibits
TLR induced
NF-kappaB and more importantly, the induction of the antiviral cytokines IFN-beta and RANTES
Premkumar et al., BMC chemical biology 2010
:
Also, the suppressive effect of triptolide on
TLR induced
NFkappaB activation was observed when either MyD88 or TRIF was knocked out, confirming that both MyD88 and TRIF mediated NFkappaB activation may be inhibited by triptolide
Chaurasia et al., Mol Cell Biol 2010
(Sepsis) :
These experiments reveal a novel PDK-1 dependent negative feedback inhibition of
TLR induced
NF-kappaB activation in macrophages in vivo
Cantu et al., Am J Transplant 2013
(Primary Graft Dysfunction) :
Three hundred sixty-two gene sets were upregulated, with eight meeting significance ( familywise-error rate, FWER p-value < 0.05 ), including the NOD-like receptor inflammasome ( NLR ; p < 0.001 ), toll-like receptors ( TLR ; p < 0.001 ), IL-1 receptor ( p = 0.001 ), myeloid differentiation primary response gene 88 ( p = 0.001 ),
NFkB activation by nontypeable Haemophilus influenzae ( p = 0.001 ),
TLR4 ( p = 0.008 ) and TLR 9 ( p = 0.018 )